CASE CONFERENCE

19th February 2018

Classidio, Devita, Hanif, Pratiwi

PAT I E N T L I S T

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Pa t i e n t L i s t
13 March 2018 (15.30-06.00)
t h

Identity Diagnosis Therapy Outcome

1 Ny. ED Preeklampsi Berat o SCTP-em Neonates Female,
01353068 superimpose pada o Inj. Cefazolin 2gr/ 24 hr 2700 gr, AS 6-8-
G1P0A0 35 yo, : 39+1 primigravida hamil o IVFD RL 12 tpm 10
weeks pregnant aterm BDP dengan o Urination catheter
1. Present pregnancy riwayat infertil primer 4
o O2 3 lpm
tahun.
o Inj. MgSO4 20% 4gr initial
dose continue with MgSO4 1
gr/ hr within 24 hr
o Nifedipin 3x10 mg if BP
>160/110
o Monitoring general
condition/VS/FHR/BC and
impending eclampsia sign
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CASE DISCUSSION

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Anamnesis

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 IDENTITY
Name : Mrs. K
Date of Birth : 05-03-1978
Address : Manyaran, Wonogiri
Occupation : Housewife
Date of Admission : 12 March 2018
No. MR : 014119xx

First Day of LMP : 15 July 2017

EDD : 20 April 2018
GA : 34+2 weeks

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Chief Complaint
Birth passage bleeding

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History of P resent Illness
Mrs. K, 40 years old, G4P2A1, pregnant 34 weeks, referral from dr.Eka,
Sp.OG (K) with diagnosis multigravide with preterm pregnancy with
section caesaria chronicles with plasenta previa sub akreta. The patient’s
chief complaint is birth passage bleeding (vlek) since 5th, 7th and 8th
gestational month
The patient believe to be pregnant 9 months, fetal movement (+), felt
uterine contraction(-) and didn’t feel regular contraction yet. No finding
of amniotic fluid leakage, blood mucus (-). Headache (-), loss of vision (-),
upper abdominal pain (-), nausea (-), vomitus (-). Urinate and defecate in
normal condition.
Antenatal care is regularly done by Obstetricians and Gynecologists.

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History of Past Illness

 Hypertension history : Denied

 Diabetes history : Denied
 Asthma history : Denied
 Allergy history : Denied
 Cardiac problem history : Denied

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History of family illness

 Hypertension history : Denied

 Diabetes history : Denied
 Asthma history : Denied
 Allergy history : Denied
 Cardiac problem history : Denied

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Obstetric history

I. Girl, 19 years, 4100 grams, SC w.i huge baby RS Warga Wonogiri

II. Girl, 13 years, spontaneous,
III. Abortus, 4 months, kuret (+) dr.Catur Sp.OG (K)
IV. Present pregnancy

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Menstuation history
Menarche : 13 y.o
Duration : 5-7 days
Cycle : regular

Marriage history
Married : 1 time
Duration : 20 years

Contraception history
Contraception (-)
Physical examination

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Physic al E x amination

 General State : Moderate ill, Compos Mentis

 Vital Sign
 Blood Pressure : 160/100mmHg
 Heart Rate : 78 x/minute
 Respiration Rate : 20x/minute
 Temperature : 36,5° C

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Physic al E x amination
Cor/pulmo within normal range Anemic conjunctiva (-/-)
Icteric Sclera (-/-)

Abdomen :
Supel, pain on fundus uteri palpation (-), single fetus,
intrauterine, longitudinal, gluteal presentation, fetus back
on the left side, head presentation still not entering
pelvic, his (-), fetal heart rate (+) 152x/min reguler,
height of fundus uteri: 32 cm.

Genital:
VT= V/U normal, vagina normal, tender portio
posterior curved, closed OUE, amnion (-) blood (-),
discharge (-)

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Laboratory Findings

 Hemoglobin : 10,0 g/dl ↓  Blood Glucose : 125 mg/dl

 Hematokrit : 34 %  HbsAg : Non reactive
 Leucocyte : 9,9 ribu/ul  Protein : +2
 Thrombocyte : 196 ribu/ul
 Erythrocyte : 4,44 juta/ul
 Blood Type :B
 PT : 11,8 detik
 APTT : 29,0 detik
 INR : 0,920

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Ultrasonography (USG)
Single fetus, intrauterine, longitudinal, gluteal presentation, fetal heart rate (+)
FB: BPD: 8,89 cm --- UK 36 weeks
HC: 31,60 cm --- UK 35 weeks
AC: 30,36 cm --- UK 36+1 weeks
FL: 6,76 cm --- UK 36+4 weeks
EFBW: 2499 gr
Placenta insertion in uterus pars anterior low segment, widening, closed
Amniotic fluid sufficient
No findings of mayor congenital anomaly

CONCLUSION
Present fetal condition is good

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Non S tress Test

Baseline 140
Variability 5-20
Acceleration (+)
Deceleration (-)
Fetal movement (+)
Contraction (-)

NST Category I

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 Diagnosis
Severe Preeclampsia, Gluteal Presentation and
Plasenta Previa Totalis at Multigravida
Preterm, Not Inpartu with history of
Sectio.Caesaria 19 years ago.
Therapy
 Conservative
 Inj. Dexamethason 1 amp/12 h IV (2 days)
 O2 3 lpm
 Inf. RL 12 dpm
 MgSO4 20% 4gram/15 min (initial dose)
 MgSO4 40% 1gram/ hr within 24 hr (continue after initial dose)
 Nifedipin 10mg/8 hr
 Monitoring general condition/VS/FHR/BC and impending eclampsia sign
 Fetomaternal staff examination (Suggestion)
 Counseling, Information, Education
 Informed Consent

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L I T E R AT U R E R E V I E W
Severe Pre-eclampsi

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DEFINITION
•Pregnancy-specific syndrome that reduce organ perfusion due to vasospasm
and endothelial activation.
•The diagnostic criteria for preeclampsia are:
• Hypertension
BP≥140/90 mmHg after 20 weeks gestation.
• Proteinuria
Proteinuria may not be a feature in some woman with the preeclampsia
syndrome, so the Task Force (2013) suggested other diagnostic criteria.
Diagnosis
 Indicators of
Preeclampsia Severity
• Headaches or visual disturbances such as

Preeclampsia Severity
scotomata
• can be premonitory symptoms of eclampsia.
• Epigastric or right upper quadrant pain and

Indicators of
elevated serum hepatic transaminase levels
• frequently accompanies hepatocellular
necrosis, ischemia, and edema that ostensibly
stretches Glisson capsule
• Thrombocytopenia
• Characteristic of worsening preeclampsia as it
signifies platelet activation and aggregation as
well as microangiopathic hemolysis.
 INCIDENCE AND RISK FACTORS

■ Maternal age (young woman>>)

■ Nulliparous

■ Multifetal gestation

■ woman with preeclampsia in the first pregnancy

■ Race and ethnicity – 5% in white, 9% in Hispanic, 11% in African-American

■ Obesity

■ Hyperhomocysteinemia

■ Metabolic syndrome
ETIOLOGY
Gestational hypertensive disorders are more likely to develop in
woman with the following characteristics:
Are exposed to chorionic villi for the first time
Are exposed to a superabundance of chorionic villi, as with
twins or hydatidiform mole
Have preexisting conditions of endothelial cell activation or
inflammation such as diabetes or renal or cardiovascular
disease
Are genetically predisposed to hypertension developing
during pregnancy.
PATHOPHYSIOLOGY
Vasospasm
– Endothelial activation causes vascular constriction with increased
resistance and subsequent hypertension.
– Endothelial cell damage causes interstitial leakage through which blood
constituents, including platelets and fibrinogen, are deposited
subendothelially.
– Ischemia of the surrounding tissues can lead to necrosis, hemorrhage,
and other end-organ disturbances characteristic of the syndrome.
PATHOPHYSIOLOGY
Cardiovascular changes
– Cardiac involvement in woman with preeclampsia is caused by
■ increased afterload due to increased peripheral resistance
■ endothelial cell damage that cause intestitial leakage, particularly in
the lung
PATHOPHYSIOLOGY
Blood volume
– Hemoconcentration has been a hallmark of severe preeclampsia and
eclampsia
– Hemoconcentration results from generalized vasoconstriction that
follows endothelial activation and leakage of plasma into the interstitial
space because of increased permeability.
PATHOPHYSIOLOGY
Hematological changes
– Thrombocytopenia
■ Defined by a platelet count < 100,000/μL
■ Delivery is advisable because thrombocytopenia usually continues
to worsen
■ After delivery, the platelet count may continue to decline for the first
day or so
■ Usually increases progressively to reach a normal level within 3 to
5 days.
– Some plasma clotting factors may be decreased
– Erythrocytes display abnormal morphology and undergo rapid
hemolysis.
PATHOPHYSIOLOGY
Kidney
– During normal pregnancy, renal blood flow and glomerular filtration rate
are increased.
– With development of preeclampsia, renal perfusion and glomerular
filtration are reduced.
– A small degree of decreased glomerular filtration may result from
reduced plasma volume, causing increased serum creatinine levels
– Abnormal values usually begin to normalize 10 days or later after
delivery
PATHOPHYSIOLOGY
Liver
– Regions of periportal hemorrhage in the liver periphery elevate serum
hepatic transaminase levels.
– It typically manifests by moderate to severe right-upper quadrant or
midepigastric pain and tenderness.
– Hemorrhagic infarction may extend to form a hepatic hematoma. These
in turn may extend to form a subcapsular hematoma that may rupture.
PATHOPHYSIOLOGY
Brain
Headaches and visual symptoms are common with severe
preeclampsia. They arise from cerebrovascular hyperperfusion that
has a predilection for the occipital lobes.
Headaches do not usually respond to analgesia, but they improve
after magnesium sulfate infusion is initiated.
There are two theories to explain cerebral abnormalities with
preeclampsia:
 Cerebrovascular overregulation in response to acute and severe
hypertension leads to vasospasm
 Sudden elevations in systemic blood pressure exceed the normal
cerebrovascular autoregulatory that leads to vasogenic edema
 PREDICTION
■ Identification of early markers of faulty placentation, impaired placental
perfusion, endothelial cell activation and dysfunction, and activation of
coagulation have a poor sensitivity for preeclampsia
■ Currently, no screening tests are predictably reliable, valid, and economical
■ Combinations of tests, some yet to be adequately evaluated, that may be
promising
PREDICTION
PREVENTION
MANAGEMENT
 MANAGEMENT
■ In severe hypertension, recommend treatment to lower systolic pressure ≤ 160
mmHg and diastolic pressure ≤ 110 mmHg.
■ Nifedipine is calcium channel blocking agent, it has recommended a 10mg-
initial oral dose to be repeated in 30 minutes if necessary.
■ The basic management objectives for any pregnancy complicated by
preeclampsia are:
– termination of pregnancy with the least possible trauma to mother and fetus
– birth of an infant who subsequently thrives
– complete restoration of health to the mother.
MANAGEMENT
■ In many woman with preeclampsia, especially those at or near term, all three
objectives are served equally well by induction of labor.
■ The treatment of severe preeclampsia is identical to that described
subsequently for eclampsia.
■ Mild cases can be managed conservatively until labor commences
spontaneously or until the cervix becomes favorable for labor induction.
■ The prime objectives are to forestall convulsions, to prevent intracranial
hemorrhage and serious damage to other vital organs, and to deliver a
healthy newborn.
MANAGEMENT
■ Early Diagnosis of Preeclampsia
– Prenatal visits every 4 weeks until 28 weeks; every 2 weeks until 36
weeks; every week until delivery; to aids early detection of preeclampsia.

■ Hospitalization
– is considered at least initially for woman with new-onset hypertension,
especially if there is persistent worsening hypertension or development of
proteinuria.
MANAGEMENT
– A systematic evaluation is instituted to include the following:
■ Detailed examination, observation for headache, visual disturbances,
epigastric pain, and rapid weight gain
■ Weight determined daily
■ Analysis for proteinuria or urine protein:creatinine ratio on admittance and
at least every 2 days thereafter
■ Blood pressure readings in the sitting position every 4 hours.
MANAGEMENT
■ A systematic evaluation is instituted to include the following:
– Measurements of plasma or serum creatinine and hepatic
aminotransferase levels and a hemogram that includes platelet
quantification. Some recommend measurement of serum uric acid and
lactic acid dehydrogenase levels and coagulation studies.
– Evaluation of fetal size and well-being and amnionic fluid volume, with
either physical examination or sonography
MANAGEMENT
■ Reduced physical activity throughout much of the day is likely beneficial
■ Absolute bed rest is not desirable.
■ Sufficient protein and calories should be included in the diet
■ sodium and fluid intake should not be limited
MANAGEMENT
■ Delayed Delivery
– Preterm severe preeclampsia are managed with conservative
management with the aim of improving neonatal outcome without
compromising maternal safety.
– Careful daily inpatient monitoring of the mother and her fetus.
MANAGEMENT
■ Termination of pregnancy
– It is the only cure for moderate or severe preeclampsia that does not
improve after hospitalization
– Labor induction is carried out, usually with intravenous oxytocin or
preinduction cervical ripening from a prostaglandin or osmotic dilator
– If induction almost certainly will not succeed or attempts have failed, then
cesarean delivery is indicated.
MANAGEMENT
■ Elective Cesarean Delivery
– Unfavorable cervix, a perceived sense of urgency because of
preeclampsia severity, and a need to coordinate neonatal intensive care,
have led some to advocate cesarean delivery.
ECLAMPSIA
■ In woman with preeclampsia, a convulsion that cannot be attributed
to another cause is termed eclampsia.
■ Depending on whether convulsion appear before, during, or after
labor, eclampsia is designated as antepartum, intrapartum or
postpartum.
■ Eclampsia is most common in the last trimester and become
increasingly frequent as term approaches.
■ Preeclampsia complicated by generalized tonic clonic convulsion
appreciably increase the risk to both mother and fetus
■ Almost without exception, but at times unnoticed, preeclampsia
precedes the onset of eclamptic convulsions.
■ Other diagnoses should be considered in woman with convulsions
more than 48 hours postpartum or in woman with focal neurological
deficits, prolonged coma, or atypical eclampsia.

■ In severe cases, coma persists from one convulsion to another, and

death may result.

■ Then can occur tacipneu, cyanosis, proteinuria, oligouria till anuria,

may be hemoglobinuria.
■ In antepartum eclampsia, labor may begin spontaneously shortly
after convulsions ensue and may progress rapidly. If the convulsions
occur during labor, contractions may increase in frequency and
intensity and the duration of labor may be shortened. Because of
maternal hypoxemia and lactic acidemia caused by convulsions, it is
not unusal for fetal bradycardia to follow a seizure.

■ Occasionally, sudden death occurs, which result from a massive

cerebral hemorrhage. Blindness with eclampsia is almost always due
to occipital lobe edema.
MANAGEMENT
Eclamptic seizures may be violent an the woman must be protected, especially her
airway.
PROTOCOL MAGNESIUM SULFATE
In aggregate, magnesium sulfate therapy associated with
significantly lower incidence of recurrent seizures compared
given an alternatife anticonvulsant. Importantly the maternal
death rate was signiicantly lower than other regimen.

Magnesium sulate is not given to treat hypertension, most likely

exerts a specific anticonvulsant action on the cerebral cortex.
PROTOCOL MAGNESIUM SULFATE

Magnesium sulphate is given as a loading dose followed by a

continuous infusion for 24 hours or until 24 hours after
delivery - whichever is the later.

The loading dose is 4g magnesium sulphate i.v. over 5 -10

minutes.

The maintenance dose is 1g magnesium sulphate i.v per hour.

PROTOCOL MAGNESIUM SULFATE

Pre-mixed magnesium sulphate is available in two preparation :

1. Magnesium sulphate 4g in 50ml. This should be
administered intravenously over 10 minutes as a loading or
bolus dose.
2. Magnesium sulphate 20g in 500ml. This should be
administered via a volumetric pump at a rate of 25ml/hour
(i.e. 1g/hour of magnesium sulphate).
SIDE EFFECTS

Motor paralysis, absent tendon reflexes, respiratory

depression and cardiac arrhythmia (increased
conduction time) can all occur but will be at a minimum if
magnesium is administered slowly and the woman is
closed monitored
IMPORTANT OBSERVATIONS

Hourly MEWS (Modified Early Warning Score) should be

recorded with the following additional observations performed :

1. Continuous pulse oximetry (alert Anaesthetist if O2 sat<95%)

and three lead ECG monitoring if available

2. Hourly urine output

3. Deep tendons reflexes (every 4 hours)

Cessation/reduction of the magnesium sulphate infusion should
be considered if:
i) The biceps reflex is not present.
ii) The respiratory rate is < 12/min.
The antidote is 10ml 10% calcium gluconate given slowly
intravenously.
Management eclampsia

Call appropriate personnel - including the resident Anesthetist.

Remember ABC.
Give the loading dose of Magnesium Sulphate 4g over 5-10
minutes intravenously and start an infusion of Magnesium
Sulphate
Diazepam may be administered if the fitting continues at the
discretion of the Anesthetist 5-10 mg intravenously.
Once stabilised the woman should be delivered.
Oximetry should be instituted if not already in place.
 Management of Reccurent fits
Give a further bolus dose of Magnesium of 2g and increase the
rate of infusion of Magnesium to 1.5g / hour.

Continue observations and consider the need for ventilation.

If two such boluses do not control seizures, then other methods

should be instituted such as the administration of conventional
anticonvulsants.
Thank You